Clinical Research
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 28, 2005; 11(24): 3719-3723
Published online Jun 28, 2005. doi: 10.3748/wjg.v11.i24.3719
Action and mechanism of Fas and Fas ligand in immune escape of gallbladder carcinoma
Li-Ning Xu, Sheng-Quan Zou, Jian-Ming Wang
Li-Ning Xu, Sheng-Quan Zou, Jian-Ming Wang, Department of General Surgery of Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Sheng-Quan Zou, Department of General Surgery of Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, 1095 Jiefang Road, Wuhan 430030, Hubei Province, China. chaoyue528@sohu.com
Telephone: +86-27-83650729 Fax: +86-27-83662398
Received: June 24, 2004
Revised: June 25, 2004
Accepted: August 5, 2004
Published online: June 28, 2005
Abstract

AIM: To study the role of Fas and Fas ligand (FasL) in biological behaviors of gallbladder carcinoma, and their correlated action and mechanism in tumor escape.

METHODS: Streptavidin-biotin-peroxidase immunohisto-chemistry technique was used to study the expression of Fas and FasL protein in 26 gallbladder carcinoma tissues, 18 gallbladder adenoma tissues, 3 gallbladder dysplasia tissues and 20 chronic cholecystitis tissues. Apoptosis of the infiltrating lymphocytes in these tissues was studied by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) method. Expression of both proteins and apoptosis of the tumor infiltrating lymphocytes in cancer tissues of primary foci was compared with clinicopathological features of gallbladder carcinoma.

RESULTS: The positive rates of Fas were not significantly different among carcinoma, adenoma, dysplasia and chronic cholecystitis. The positive rate of FasL in carcinoma was significantly higher than that in chronic cholecystitis (χ2 = 4.89, P<0.05). The apoptotic index (AI) in carcinoma was significantly higher than that in adenoma (t’ = 4.19, P<0.01) and chronic cholecystitis (t’ = 8.06, P<0.01). The AI was significantly lower in well-differentiated carcinoma and Nevin I-III carcinoma than that in poorly-differentiated carcinoma (t’ = 2.63, P<0.05) and Nevin IV-V carcinoma (t’ = 3.33, P<0.01). The confidence interval (CI) of infiltrating lymphocytes in adenoma, chronic cholecystitis, well-differentiated carcinoma and Nevin I-III carcinoma was very significantly lower than that in carcinoma (t’ = 6.99, P<0.01), adenoma (t’ = 3.66, P<0.01), poorly-differentiated carcinoma (t’ = 5.31, P<0.01) and Nevin IV-V carcinoma (t’ = 3.76, P<0.01), respectively. The CI of apoptosis of infiltrating lymphocytes in well-differentiated carcinoma was significantly lower than that in poorly-differentiated carcinoma (t = 2.52, P<0.05), and was not significantly lower in Nevin I-III carcinoma than in Nevin IV-V carcinoma (t = 1.42, P>0.05). Apoptosis of infiltrating lymphocytes was not discovered in adenoma and chronic cholecystitis.

CONCLUSION: FasL expressed in gallbladder carcinoma cells permits tumor cells to escape from immune surveillance of organism by inducing apoptosis in infiltrating lymphocytes of carcinoma tissues. Up-regulation of FasL expression plays an important role in invasive depth, histological classification and metastasis of gallbladder carcinoma.

Keywords: Fas; Fas ligand; Immune escape; Gallbladder carcinoma